Dietary caloric restriction provides the only known method to extend mean and maximal lifespan and to delay the onset of a variety of late-life diseases. The applicant recently used 21 percent moderate dietary caloric restriction regimes in the first successful attempt to delay senile-type cataract as modeled in the Emory mouse (22). Preliminary studies with 40 percent dietary caloric restriction show even more impressive retardation of cataract. Elucidation of the mechanisms by which caloric restriction results in delayed cataract would allow unique opportunities to delay human cataract without the extreme, and questionably pleasurable, changes in eating patterns. Such information should also help set directions for future cataract research. The Emory mouse is a useful model in which to study the mechanisms by which dietary restriction prolongs lens clarity because it develops cataracts which, like human cataracts, are of post-maturity onset and which originate primarily but not exclusively in the lens nucleus. These cataracts also show many biochemical and morphological similarities to human cataracts. (**Depleted: comparisons between C3B mice and Emory mice.) The applicant and his coworker's initial studies of lens proteins suggest that caloric restriction is associated with extended maintenance of protein integrity, perhaps involving prolonged antioxidant and/or proteolytic capabilities. It is also associated with diminished plasma glucose, glycohemoglobin and diminished lens protein-glycation (nonenzymatic glycosylation). Excessive bodily DNA damage is not suggested in our preliminary studies. Thus, they would study relationships between the delay of cataract and a) antioxidant and/or; b) proteolytic capabilities; c) protein glycation; and d) DNA damage as they are affected by aging and caloric restriction. Parts of studies c and d would be done with collaborators. Since diabetics are known: 1) to have higher circulating glucose; 2) to have four times the incidence of cataract at young ages; and 3) to have many of the same types of protein damage in their lenses as is seen in senile cataracts, it is probable that their conclusions would lead to ways to delay both senile and diabetic cataract.